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183 11606 Ensembl ENSG00000135744 ENSMUSG00000031980 UniProt P01019 P11859 Q3UTR7 RefSeq (mRNA) NM_000029 NM_001382817 NM_001384479 NM_007428 RefSeq (protein) NP_000020 NP_001369746 NP_031454 Location (UCSC) Chr 1: 230.69 – 230.75 Mb Chr 8: 125.28 – 125.3 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Angiotensin is a peptide hormone that causes vasoconstriction and an increase ...
Angiotensin II is the major bioactive product of the renin–angiotensin system, binding to receptors on intraglomerular mesangial cells, causing these cells to contract along with the blood vessels surrounding them; and to receptors on the zona glomerulosa cells, causing the release of aldosterone from the zona glomerulosa in the adrenal cortex.
Changes in renin ultimately alter the output of this system, principally the hormones angiotensin II and aldosterone. Each hormone acts via multiple mechanisms, but both increase the kidney's absorption of sodium chloride , thereby expanding the extracellular fluid compartment and raising blood pressure.
increase in plasma angiotensin II, ACTH, or potassium levels, which are present in proportion to plasma sodium deficiencies. (The increased potassium level works to regulate aldosterone synthesis by depolarizing the cells in the zona glomerulosa, which opens the voltage-dependent calcium channels.) The level of angiotensin II is regulated by ...
There are many classes of antihypertensives, which lower blood pressure by different means. Among the most important and most widely used medications are thiazide diuretics, calcium channel blockers, angiotensin-converting enzyme inhibitors (ACE inhibitors), angiotensin II receptor blockers or antagonists (ARBs), and beta blockers.
The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II.The activated receptor in turn couples to G q/11 and G i/o and thus activates phospholipase C and increases the cytosolic Ca 2+ concentrations, which in turn triggers cellular responses such as stimulation of protein kinase C.
It is stimulated by angiotensin II and aldosterone, and inhibited by atrial natriuretic peptide. It is very efficient, since more than 25,000 m mol /day of sodium is filtered into the nephron , but only ~100 mmol/day, or less than 0.4% remains in the final urine.
Contrastly, TXA 2 vascular tissue synthesis is stimulated by angiotensin II which promotes cyclooxygenase I's metabolism of arachidonic acid. An angiotensin II dependent pathway also induces hypertension and interacts with TXA 2 receptors. [6]